Vitamin deficiencies can cause neurological manifestations. Cobalamin (vitamin B12) deficiency results in subacute combined degeneration, presenting with paresthesias, weakness, and spinal cord lesions. Folate deficiency causes similar symptoms. Vitamin E deficiency leads to spinocerebellar degeneration. Pellagra due to niacin deficiency can cause diarrhea, dermatitis, dementia, and other neurological symptoms. Pyridoxine deficiency can cause seizures in infants or neuropathy in adults. High doses of pyridoxine supplementation itself can cause neuropathy. Timely treatment of deficiencies can improve or stabilize neurological symptoms.

1. VITAMINS
AND
NERVOUS SYSTEM
Dr. Sunil Kumar Sharma
Senior Resident
Dept. of Neurology
GMC Kota

2. INTRODUCTION
• Vitamin – organic vital nutrient - required in limited amounts
for normal growth and development .
• Organism cannot synthesize in sufficient quantities
• Must be obtained through the diet
• Fat soluble - DEKA
• Water soluble - BC

3. VITAMIN DEFICIENCY
• Dietary insufficiency - Poor intake
- Chronic alcoholism
• Malabsorption due to gastrointestinal diseases
• Bariatric surgery
• Others - growth, infection, and pregnancy

4. NEUROLOGICAL MANIFESTATIONS OF VITAMIN
DEFICIENCY

5. IMPORTANT VITAMINS

6. COBALAMIN (VITAMIN B12)
• Abundant in meat, fish, and most animal byproducts.
• Strict vegetarians seldom develop symptoms
• Adequate amount is available in legumes
• Normal serum levels - 200 ng/L to 1000 ng/L.
• RDA - 2.4 μg/day,.

7. COBALAMIN (VITAMIN B12)
• Intestinal absorption - binds to intrinsic factor- by gastric
parietal cells – ileum – transcobalamin - tissue.
• 1% to 5%, also absorbed without intrinsic factor
• 90% - stored in the liver
• Many years are needed to deplete the body store.
• A clinical relapse in pernicious anemia – may takes an average
of 5 yrs.

8. ROLE
Two biochemical reactions depend on cobalamin-
• (A)-As precursor in the conversion of methylmalonyl
coenzyme-A (co-A) to succinyl co-A.
It’s importance to the nervous system is unclear.
• (B)-Folate-dependent reaction in which the methyl group
of methyl-THF is transferred to homocysteine to yield
methionine and THF.
• Used as a cofactor for methionine synthase.
• Methionine → SAM - used for methylation reactions in
the nervous system.

10. CAUSES OF DEFICIENCY
• Defective intrinsic factor production by parietal cells - P.
Anemia
• AB to PCs or lymphocytic infiltrations of the gastric mucosa
• Food-cobalamin malabsorption - cobalamin remains bound
and cannot be absorbed even in the presence of available
intrinsic factors.
Dali-Youcef, N., Andres, E., 2009. An update on cobalamin deficiency in adults. QJM. 102, 17–28.

11. PREDISPOSING FACTORS
• Atrophic gastritis and hypochlorhydria
• H. Pylori infection
• Gastrectomy or other gastric surgeries
• Intestinal bacterial overgrowth
• Prolonged use of PPIs.
• Biguanides (e.G., Metformin).

12. B12…
• HIV Pt. - often have low serum B12, with N homo. & MMA
• N2O abuse – similar clini. syndrome of myeloneuropathy
• Mechanism - interference with homocysteine to methionine
• Prolonged exposure is necessary in N. individuals
• B12 Deficient Pt. -brief exposures during GA
• Subacute onset after Sx.- resolve quickly Rx.

13. CLINICAL FEATURES
• Insidious onset with paresthesias in the hands or feet
• Weakness and unsteadiness of gait
• L’hermitte sign may be present.
• Mental slowing, depression, confusion, delusions, and
hallucinations are common.
• Occasionally pt. present with only cognitive or psychiatric
symptoms.

14. O/E-
• Signs of both peripheral nerve and spinal cord involvement
• Loss of vibration(most consi.) or joint position sense (severe)
• DTR – Variably affected, Romberg sign may be present.
• Motor impairment-most severe in the legs
• Visual impairment may antedate other manifestations
• B/L visual loss, optic atrophy, and centrocecal scotoma.
• Brainstem or cerebellar signs, chorea, autonomic
insufficiency, or even reversible coma may rarely occur

15. LABORATORY STUDIES
• Blood cobalamins -bound to two transport proteins,
transcobalamin and haptocorrin.
• Bound to transcobalamin- k/a holotranscobalamin –
• Fraction available to tissues
• Accounts for 10% to 30% of the serum level measured by
standard laboratory methods.
• Falsely N. level- Myeloproliferative and hepatic disorders ↑
haptocorrin
• Falsely low- pregnancy, contraceptives , Folate deficiency

16. • Homocysteine level - fasting or after an oral methionine load.
• Blood sample should be refrigerated immediately - level may
↑ at room temperature for several hours.
• ↑ homocysteine and MMA are not specific for B12 deficiency
• In B12 deficient pt. - levels normalize within 2 weeks of Rx.
ELEVATED METHYLMALONIC
ACID
Cobalamin deficiency
Renal insufficiency
Inherited metabolic disorders
Hypovolemia
ELEVATED HOMOCYSTEINE
Cobalamin deficiency
Folate deficiency
Pyridoxine deficiency
Renal insufficiency
Hypothyroidism
Psoriasis
Inherited metabolic disorders
Hypovolemia

17. • Hemato. abn. may be absent at the time of neuro. presentation
• Imaging -MRI may be normal, or T2-signal abnormalities may
be seen in the lateral or posterior columns in SACD, GAD+
• Encephalopathy or dementia - multiple foci of T2 signal
abnormalities in the deep WM- may become confluent
• DTI may be more sensitive - that correlate with cogni. dysfun.
• NCS- small or absent sural nerve sensory potentials ≈ 50% -
axonal polyneuropathy.
Kumar, A., Singh, A.K., 2009. Teaching NeuroImage: Inverted V sign in subacute combined degeneration of spinal cord. Neurology 72, e4.
Gupta, P.K., Gupta, R.K., Garg, R.K., et al., 2014. DTI correlates of cognition in conventional MRI of normal-appearing brain in patients with clinical features of subacute
combined degeneration and biochemically proven vitamin B12 deficiency. Am. J. Neuroradiol. 35, 872–877

18. Demyelination and loss of axons are more
widespread in posterior than in lateral
columns
Gadolinium-enhanced, T1-
weighted cervical and upper
thoracic magnetic resonance image
showing marked enhancement of
posterior cord of a 30-year-old
woman

19. INVERTED V /RABBIT EAR SIGN
Transverse T2-weighted MR image of the cervical spinal cord at C2
level demonstrates bilateral symmetric signal intensity within the
dorsal columns (inverted V sign)

20. PATHOLOGY
• Microscopically-spongiform changes in the WM of spinal cord.
• Most severely affected – post. columns at the cervical and
upper thoracic levels .
• Pathological changes also common in the lateral columns
• Anterior columns involvement rare -advanced cases.
• PNS- axonal degeneration- in some demyelination.
• Involve. of the optic nerve and cerebral WM also occurs.

21. TREATMENT
• A typical regimen –1000 μg / IM daily for first week, followed by
1000 μg weekly for 1 month, and monthly injections thereafter.
• High doses of cobalamin appear to be safe
• Oral - 1000 μg daily - some success- close monitoring
• Neurological improvement – delayed / may be incomplete.
• Symptomatic improvement - first 6 to 12 months of therapy.
• Remission correlates inversely with the time lapse between onset
of symptoms and initiation of therapy.

22. FOLATE DEFICIENCY
• Folate def.- same neurological deficits as cobalamin deficiency
• RDA-400 μg/day.
• Central role in the biosynthesis of methionine, SAM & THF
• Absorption - jejunum > ileum.
• Def. - Chronic alcoholism , Small-bowel disease (e.g., sprue,
Crohn disease, UC) , Pregnant women and AED, Sulfasalazine,
MTx , triamterene, and OCP

23. CLINICAL FEATURES
• Majority of Pt. with ↓ folate don’t have overt neuro. findings
• C/P- similar to SACD -limb paresthesias, weakness, and gait
unsteadiness.
• Megaloblastic anemia, impaired position and vibration sense,
pyramidal signs, and possibly dementia.
• Chronic folate deficiency – MCI or ↑ stroke risk in adults.
• Low folate level - depression and cognitive impairment.
• Increased frequency of NTDs in babies

24. Laboratory Studies-
• Plasma and erythrocyte(more reliable) folate levels .
• S. homocysteine ↑ in folate deficiency.
Treatment
• Initially 1 mg several times per day f/b a maint. dose of 1
mg/day.
• For acutely ill patients, parenteral doses of 1 to 5 mg .
• with oral doses as high as 15 mg/day-no report of toxicity.
• WWE of childbearing potential - 0.4 mg or more
• 5 mg /day in pregnant WWE on AED

25. VITAMIN E
• Vitamin E - a group of tocopherols and tocoretinols- α-
tocopherol is the most important.
• Free-radical scavenger and an antioxidant
• Potential role in the prevention and treatment of a wide
range of neurological diseases.
• value of vitamin E for these indications has yet to be proven.

26. Causes of Vitamin E Deficiency

27. Abetalipoproteinemia or Bassen–Kornzweig syndrome
• AR disorder - mutation in the MTTP gene(Micro. Trigly. trans.
protein) - impaired absorption of fat and fat-soluble vitamins
• Vit. E and cholesterol –Low, apolipoprotein B-absent.
• Acanthocytes and retinal pigment changes are characteristic.
• Dx. –serum lipoprotein electroporesis
• Rx.- Vitamin supplements
Zamel, R., Khan, R., Pollex, R.L., et al., 2008. Abetalipoproteinemia: two case reports and review of the literature. Orphanet J. Rare Dis. 3, 19.

28. Familial hypobetalipoproteinemia-
• Variable degrees of malabsorption and symptoms, and about
50% are due to mutation in the APOB gene (Peretti et al.,
2010).
Peretti, N., Sassolas, A., Roy, C.C., et al., 2010. Guidelines for the diagnosis and management of chylomicron retention disease based on a review of the literature and the
experience of two centers. Orphanet J. Rare Dis. 5, 1.

29. ATAXIA WITH ISOLATED VITAMIN E DEFICIENCY
(AVED)-
• Childhood onset ,AR ataxia
• Mutations in the α-tocopherol transfer protein gene (TTP) on
chromosome 8q
• Neuronal deg.-purkinje cells, RP, PN with ataxia(≈FA)
• Vit. E < 1.8 mg/L.
• Rx- High dose Vit. E

30. CLINICAL FEATURES OF VIT. E DEF.
• Clinical symptoms - do not begin until many years of
malabsorption deplete the vitamin reserves.
• 15 to 20 years in adults, but 1 to 2 years in children
• C/P- weakness or gait unsteadiness.
• Neuro. exa. reveals a syndrome of spinocerebellar
degeneration with PN.
• Some patients are diagnosed erroneously with Friedreich
ataxia.

31. Most consistent abnormalities are-
• Limb ataxia
• Areflexia,
• Loss of vibration and position sense.
• Cutaneous sensation-usually spared or affected to a lesser
degree.
• Nystagmus, ptosis, or partial external ophthalmoplegia.
• Myopathy in some pt.
• Babinski sign may be present.

32. LAB. STUDIES-
• Dx.- appropriate neuro. syndrome+ low serum vitamin E
• Others -Stool fat ↑ , s. carotene conc. often ↓, both
reflecting fat malabsorption.
• CSF - normal.
• NCS-sensory polyneuropathy, motor conduction abnormality
and features of a demyelinating neuropathy rare (Puri et al.,
2005).
• There may be high signal lesions in the posterior columns on
T2-weighted MRI

33. Treatment
• RDA - 10 mg (equivalent to 10 IU) of DL-α-tocopherol.
• Improvement/stabilization, of neuro. Status possible,
even in hereditary diseases (El Euch-Fayache et al., 2014;
Peretti et al., 2010
• No consensus on the optimal therapeutic dosage - from
200 mg/day to 100 mg/kg/day.
• begin therapy with 200 to 600 mg/day - if no
improvement - higher oral dosages or parenteral
• Bile salts Supplementation - in intestinal malabsorption.

34. PELLAGRA (NICOTINIC ACID DEFICIENCY)
• Nicotinic acid/Niacin is converted to - NAD and NADP.
• Dietary deficiency - pellagra (Italian pelle agra- “rough skin”).
• Pellagra - who consume primarily corn.
• Corn lacks nicotinic acid as well as tryptophan
• Affects three organ systems : GI tract, skin, and nervous
system ( mnemo. of “three Ds”: diarrhea, dermatitis, and
dementia).

35. • The neurological syndrome of pellagra is not well defined.
• Reported cases, sp. of alcoholic pellagra, frequently
confounded by other coexisting CNS disorders such as WE.
• C/P- neuropsychiatric (e.g., irritability, apathy, depressed
mood, inattentiveness, memory loss) and stupor or coma.
• Spasticity, Babinski sign, gegenhalten, and startle myoclonus
• The diagnosis of nonendemic pellagra(alcoholism or
malabsorption) can be made only on clinical grounds

36. • No available method for blood niacin level determination.
• Under-recognized and mistaken for other causes of
encephalopathy e.g.CJD (Kapas et al., 2012).
• RDA- 6.6 mg/1000 kcal dietary intake.
• Rx-Oral nicotinic acid in -50 mg several times a day
• Alternatively, parenteral 25 mg -2 to 3 times/day.
Kapas, I., Majtenyi, K., Toro, K., et al., 2012. Pellagra encephalopathy as a differential diagnosis for Creutzfeldt-Jakob disease. Metab. Brain Dis. 27, 231–235.

37. VITAMIN B6 (PYRIDOXINE)
• 3 naturally occurring compounds— pyridoxine, pyridoxal and
pyridoxamine
• All three converted to pyridoxal-5’-phosphate (PLP), the
biologically active coenzyme.
• Infantile sz.- MC - breastfeeding by malnourished mothers .
• C/P- Normal birth history and are entirely healthy
• Hyperirritability ,exaggerated auditory startle.
• Recurrent convulsions and may have SE.

38. • Once the dietary insufficiency is corrected, patients become
free of seizures and develop normally.
• Another rare form of pyridoxine-responsive seizure occurs in
infants.
Two related causes-
1- Mutation of the ALDH7A1 gene- ↓ enzyme antiquitin-
inactivation of PLP.
2- Def. of Pyridoxamine phosphate oxidase (PNPO) – imp. in the
synthesis of PLP (Pearl and Gospe, 2014).
• Seizures during the neonatal period, respond poorly to
anticonvulsants.
• Long-term , large amounts of pyridoxine or PLP is needed .

39. • Adults are more tolerant of vitamin B6 deficiency.
• In adults, chronic deficiency -subacute or chronic neuropathy.
• INH , hydralazine, and penicillamine
• Sensory symptoms starts distaliy from feet-proximally
• Burning pain is disabling in some instances.
• O/E- distal weakness, depressed DTR , and impaired distal
sensation
• In pt. taking isoniazid, pyridoxine supple. of 50 mg/day .

40. • Indiscriminate use of pyridoxine supple. may be harmful.
• High doses of pyridoxine (1000 mg/day or more) can reliably
cause a sensory neuropathy within a few months (Berger et
al., 1992).
• C/P- sensory ataxia with impaired sensation, areflexia, and
Romberg sign.
• Limit the daily dosage to 50 mg or less
Berger, A.L., Schaumburg, H.H., Schroeder, C., et al., 1992. Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study
of pyridoxine neurotoxicity. Neurology 42, 1367–1370

41. THIAMINE(B1)
• Crucial role in the meta. of carbo., amino acids, and lipids.
• Absorbed in the jejunum and ileum
• A continuous dietary supply is necessary
• Demand ↑ with high glucose intake , during pregnancy and
many systemic illnesses.
• The mini. daily require. - 0.3 mg/1000 kcal ,RDA-1.2 mg
• For therapeutic purposes, a target of 50 to 100 mg/day is
often used.

42. • Diagnosis - appropriate clinical features + nutritional
deficiency / high metabolic demands.
• B1 in serum and urine ↓ but do not reliably reflect tissue
concentrations.
• Erythrocyte transketolase activity level - dependent on
thiamine and provides an assay of functional status.
• Pyruvate accumulates during thiamine deficiency- additional
confirmation.
• A blood sample should be drawn before initiation of
treatment -laboratory abnormalities normalize quickly.

43. THIAMINE DEFICIENCY NEUROPATHY
(BERIBERI)
• Beriberi literally means extreme weakness.
• Affects heart and peripheral nerves - congestive
cardiomyopathy, sensorimotor polyneuropathy, or both.
• The classical wet and dry forms
• The neuropathy generally develops over weeks or months.
• Pt. C/O - paresthesias or pain in the feet.

44. • MC neurological finding is distal sensory loss.
• Weakness appears first in the finger and wrist extensors and
the ankle dorsiflexors.
• Ankle stretch reflexes - lost in most patients.
• When cardiac dysfunction is present- tachycardia,
palpitations, dyspnea, fatigue, and ankle edema

45. • Electrodiagnostic studies – Sensori-motor axonal
neuropathy with neuropathic changes on electromyography.
• Electrocardiographic or other cardiac abnormalities may be +
• Thiamine, 100 mg IV in the acute stage- if there is doubt
about adequate GI abso.
• Long-term Rx - balanced diet with oral supple. of thiamine
and other vitamins.
• Gradual return of sensory and motor function - may take
many months and may be incomplete.

46. INFANTILE BERIBERI
• An acute syndrome of thiamine deficiency in infants
• Rice-eating populations of Asia, MC in breastfed infants
• B1 often deficient in breast milk from mothers who eat
primarily polished rice.
• It bears little resemblance to the adult form
• Acute cardiac symptoms are common, often preceded by a
prodrome of anorexia, vomiting, deficient weight gain, and
restlessness.
• Dyspnea, cyanosis, and signs of heart failure , can lead rapidly
to death.

47. • Arytenoid edema and recurrent laryngeal neuropathy may
give rise to hoarseness, dysphonia, and eventually aphonia.
• Early signs of coughing and choking may be mistaken for
respiratory tract infections.
• Central nervous system manifestations include drowsiness,
ophthalmoplegia, and convulsions.
• often begin abruptly and carry a grave prognosis.
• If given promptly, parenteral 5 to 20 mg of thiamine can be
life saving.

48. • In 1881, Carl Wernicke described a syndrome of mental
confusion, ophthalmoplegia, and gait ataxia in three patients,
two of whom were alcoholics.
• At autopsy - multiple small hemorrhages were seen in the
periventricular gray matter, primarily around the aqueduct
and the third and fourth ventricles.
• Shortly after Wernicke’s ,Korsakoff, a Russian psychiatrist,
described an amnesia syndrome in 20 alcoholic men.

49. WERNICKE–KORSAKOFF SYNDROME
• Korsakoff syndrome and Wernicke encephalopathy are
different stages of one disease process (Wernicke– Korsakoff
syndrome).
• Korsakoff syndrome typically follows Wernicke ence.
• Wernicke encephalopathy -thiamine deficiency due to
chronic alcoholism(MC)
• Other conditions- poor nutritional state, from inadequate
intake, malabsorption, or increased metabolic requirement
• Wernicke encephalopathy may be precipitated acutely by IV
glucose administration or carbohydrate loading in at risk pt.

50. ASSOCIATED CONDITIONS IN NON-ALCOHOLIC
PATIENTS WITH WERNICKE ENCEPHALOPATHY

51. • Classic triad in WE - confusion, ophthalmoplegia & ataxia(GOA)
• All three elements - in only about 1/3
• Confusion- MC symptom and develops over days or weeks.
• Characterized by - inattention, apathy, disorientation, and
memory loss. Stupor or coma is rare.
• Gait ataxia is likely a result of cerebellar abnormality,
neuropathy, and vestibular dysfunction.
• O/E- truncal ataxia - similar to alcoholic cerebellar deg.

52. • Ophthalmoplegia, - commonly involves both lateral recti, +/-
other extraocular muscles
• Horizontal nystagmus on lateral gaze, ,vertical nystagmus
• Symmetrical involvement of periventricular structures at the
level of the third and fourth ventricles.
• Lesions of the nuclei of cranial nerves III, VI, and VIII -eye
findings.
• Other - hypothermia and postural hypotension-involvement
of hypothalamic and brainstem autonomic pathways.

53. • Korsakoff syndrome follows repeated bouts of
encephalopathy or an inadequately treated acute
encephalopathy.
• The memory impairment is out of proportion to other
cognitive dysfunction - both anterograde and retrograde
amnesia.
• Severe difficulty establishing new memories, always coupled
with a limited ability to recall events that antedate the onset
of illness by several years.
• C/P- disoriention to time and place.
• Alertness, attention, social behavior, and most other aspects
of cognitive functioning are relatively preserved.

54. • Confabulation can be a prominent feature sp. in the early
stages
• The memory disorder -lesions for the diencephalon and
temporal lobes.
• Injury to these regions, regardless of cause (e.g., infarction,
trauma, tumors, herpes encephalitis), can produce a
syndrome indistinguishable from the amnesia syndrome seen
in alcoholic patients

55. LABORATORY STUDIES
• Brain MRI helpful - shows signal abnormalities on T2-
weighted FLAIR and diffusion-weighted images,
symmetrically distributed around the periaqueductal regions,
tectal plates, medial thalami, and bilateral mammillary
bodies.
• Other regions such as the cerebellar vermis, pons, medulla,
dentate nuclei, cranial nerve nuclei, and basal ganglia are at
times affected.
• Some lesions may show contrast enhancement.
• Hemorrhages are rarely seen.

56. • CT head - is much less sensitive
• MRI signal abN- resolve completely with prompt treatment
• Shrunken mammillary bodies - late residual finding.
• The CSF- N or mild elevation in protein.
• Serum thiamine level and erythrocyte transketolase activity
may be depressed, and there may be an elevation of serum
pyruvate.

57. Pathology
• The pathological process depends on the age of the lesions.
• Macroscopically, varying degrees of congestion, petechial
hemorrhages, shrinkage, and discoloration are present
• Glial proliferation and myelin pallor characterize the more chronic
lesions.
• The regions affected - same as involved on MRI.
• WE- preventable and treatable.
• The under-recognition d/t overemphasis on alcoholism as a cause
or a misconception that all three elements of the clinical triad are
needed for a diagnosis.
• Wernicke encephalopathy occurring under other settings may be
mistaken for -uremia, sepsis, or other systemic diseases.

58. Treatment
• WE should be suspected in all patients with encephalopathy
and at risk for nutritional deficiency (Galvin et al., 2010).
• Treatment should not be delayed
• Intravenous thiamine is safe, inexpensive, and effective
• Should receive thiamine before administration of glucose to
avoid worsening.
• 500 mg IV in the acute stage, f/b 100 mg 3 times daily during
the first week.
• Parenteral administration is preferable over oral supplements
• If left untreated, Wernicke encephalopathy is progressive.

59. • With Rx the majority of ocular signs resolve within hours,
• Fine horizontal nystagmus persists in approx. 60% of pt.
• The gait disturbance resolves slowly - 1/3 may have gait
abnormality even months after treatment.
• As the global confusional state recedes, some patients are left
with the Korsakoff syndrome.
• Rx of Korsakoff syndrome is usually limited to social support.
• Treating with AChEI or memantine- controlled studies did not
show a consistent benefit (Luykx et al., 2008).

60. VITAMIN A
• vitamin A def. is uncommon in Europe and the US
• Deficiency - fat malabsorption syndromes such as sprue,
biliary atresia, and cystic fibrosis.
• The earliest sign - reduced ability to see in dim light.
• Retinol, an aldehyde form of vitamin A, binds with the
protein, opsin, to form rhodopsin, which is responsible for
vision at low light level.
• Xerosis, or keratinization, of the conjunctiva and cornea often
accompanies night blindness.

61. • characteristic Bitot spots in some pt. ,if severe, can lead to
permanent blindness.
• Chronic daily consumption of >25,000 IU may produce toxicity
• Serum retinol - accepted lower limit of normal is 20 mg/dL,
>100 mg/dL are suggestive of toxicity.

62. VITAMIN C
• Ascorbate (vitamin C) -vital antioxidant molecule in the brain
• Transported into the brain and neurons via the Sodium-
dependent Vitamin C Transporter-2 (SVCT2)
• Ascorbate is proposed as a neuromodulator of glutamatergic,
dopaminergic, cholinergic and GABAergic transmission
• Neurodegenerative diseases - high levels of oxidative stress
Vit C is posited to have potential therapeutic roles

63. VITAMIN D
• Vitamin D def.- dietary insufficiency, inadequate sunlight
exposure, immobility, anticonvulsant use, malabsorption,
hypophosphatemia, and hyperparathyroidism.
• 25-hydroxyvitamin D. Levels below 10 ng/mL indicate
deficiency
• 10 and 20 ng/mL suggest some degree of insufficiency.
• 50% of the elderly population may have insufficient amounts
• vitamin D has potentially diverse effects in the nervous
system through its action on inflammatory cytokines,
neurotrophins, and calcium-binding proteins.

64. • The best-documented syndrome -myopathy characterized by
proximal weakness (Al-Said et al., 2009).
• Progressive weakness develops over many months.
• When severe, some patients are wheelchair dependent.
• Diffuse bone pain, muscle pain, or back pain is common.
• Stretch reflexes and sensation are normal.
• Serum creatine kinase level is usually normal or only mildly
elevated.
• Serum alkaline phosphatase is abnormally high, and calcium
and phosphorus may be normal or mildly decreased.

65. • EMG shows short-duration low-amplitude and polyphasic motor
unit potentials without spont. activities.
• Nonspecific type II muscle fiber atrophy - on biopsy.
• Initial treatment - vitamin D (cholecalciferol, 800 international units
daily) and dietary calcium (1200 mg daily).
• The underlying causes – s/b identified and corrected if possible.
• Dietary supplementation is continued for several months even after
correction of the underlying cause.
• Once therapy is instituted, pain subsides, and laboratory
abnormalities return to normal after a short period of Rx
• Recovery of muscle weakness follows over the subsequent months

66. Thank you

67. REFERENCES
• Bradley’s neurology in clinical practice ; 7th ed.
• DIAGNOSTIC IMAGING: SPINE; Jeff Ross et. al.
• Harrison’s principles of internal medicine ; 19th ed.
• Radiopedia.com
• Inverted V sign in subacute combined degeneration of spinal
cord; Ashok Kumar, MD,DM,Amar Kumar Singh;
10.1212/01.wnl.0000338663.59433.9c Neurology 2009;72;e4
• Vitamin C Function in the Brain: Vital Role of the Ascorbate
Transporter (SVCT2)FIONA ET AL